All Relations between hypertrophic and matrix compartment

Publication Sentence Publish Date Extraction Date Species
Marcy Wong, Mark Siegrist, Kelly Goodwi. Cyclic tensile strain and cyclic hydrostatic pressure differentially regulate expression of hypertrophic markers in primary chondrocytes. Bone. vol 33. issue 4. 2004-07-06. PMID:14555274. the goal of this study was to test this hypothesis by examining the expression of hypertrophic chondrocyte markers (transcription factor cbfa1, mmp-13, type x collagen, vegf, ctgf) and cartilage matrix proteins under cyclic tension and cyclic hydrostatic pressure. 2004-07-06 2023-08-12 Not clear
Young-Sook Kim, Marpadga A Reddy, Linda Lanting, Sharon G Adler, Rama Nataraja. Differential behavior of mesangial cells derived from 12/15-lipoxygenase knockout mice relative to control mice. Kidney international. vol 64. issue 5. 2004-06-24. PMID:14531803. the 12/15-lipoxygenase (12/15-lo) enzyme has been implicated in the pathogenesis of diabetic nephropathy since lipoxygenase products induce cellular hypertrophy and extracellular matrix deposition in mesangial cells. 2004-06-24 2023-08-12 mouse
Nan Jia, Hiroshi Okamoto, Toshihiro Shimizu, Satoru Chiba, Yutaka Matsui, Takeshi Sugawara, Masatoshi Akino, Akira Kitabatak. A newly developed angiotensin II type 1 receptor antagonist, CS866, promotes regression of cardiac hypertrophy by reducing integrin beta1 expression. Hypertension research : official journal of the Japanese Society of Hypertension. vol 26. issue 9. 2004-06-24. PMID:14620930. previous studies have demonstrated that integrins link the extracellular matrix to the hypertrophic response pathway of cardiac myocytes in vitro. 2004-06-24 2023-08-12 rat
Céline Colnot, Chuanyong Lu, Diane Hu, Jill A Helm. Distinguishing the contributions of the perichondrium, cartilage, and vascular endothelium to skeletal development. Developmental biology. vol 269. issue 1. 2004-06-14. PMID:15081357. during the initiation of endochondral ossification three events occur that are inextricably linked in time and space: chondrocytes undergo terminal differentiation and cell death, the skeletal vascular endothelium invades the hypertrophic cartilage matrix, and osteoblasts differentiate and begin to deposit a bony matrix. 2004-06-14 2023-08-12 mouse
Céline Colnot, Chuanyong Lu, Diane Hu, Jill A Helm. Distinguishing the contributions of the perichondrium, cartilage, and vascular endothelium to skeletal development. Developmental biology. vol 269. issue 1. 2004-06-14. PMID:15081357. endothelial cells residing within the perichondrium are the first cells to participate in the invasion of the hypertrophic cartilage matrix, followed by endothelial cells derived from the host environment. 2004-06-14 2023-08-12 mouse
Philippe H Tartaix, Marie Doulaverakis, Anne George, Larry W Fisher, William T Butler, Chunlin Qin, Erdjan Salih, Melin Tan, Yukiji Fujimoto, Lyudmila Spevak, Adele L Boske. In vitro effects of dentin matrix protein-1 on hydroxyapatite formation provide insights into in vivo functions. The Journal of biological chemistry. vol 279. issue 18. 2004-06-10. PMID:14769788. dentin matrix protein-1 (dmp1) is a mineralized tissue matrix protein synthesized by osteoblasts, hypertrophic chondrocytes, and ameloblasts as well as odontoblasts. 2004-06-10 2023-08-12 mouse
A Bakr M Rabie, Guo Hua Tang, Urban Häg. Cbfa1 couples chondrocytes maturation and endochondral ossification in rat mandibular condylar cartilage. Archives of oral biology. vol 49. issue 2. 2004-06-07. PMID:14693204. quantitative analysis demonstrated that both types of cbfa1 proteins reached their maximum level on day 56, which coincided with the terminal maturation of hypertrophic chondrocytes and the aggregation of mineralisation deposits in extracellular matrix. 2004-06-07 2023-08-12 rat
Tatyana V Dudnakova, Vladimir L Lakomkin, Valerie G Tsyplenkova, Boris V Shekhonin, Vladimir P Shirinsky, Valeri I Kapelk. Alterations in myocardial ultrastructure and protein expression after a single injection of isoproterenol. Molecular and cellular biochemistry. vol 252. issue 1-2. 2004-06-03. PMID:14577591. obtained results indicate that even a single injection of isoproterenol creates long lasting structural alterations in cardiac muscle accompanied by the increased expression of extracellular matrix proteins and several sarcoplasmic proteins apparently involved in hypertrophic response of cardiomyocytes. 2004-06-03 2023-08-12 rat
Jennifer L Gooch, Yves Gorin, Bin-Xian Zhang, Hanna E Abbou. Involvement of calcineurin in transforming growth factor-beta-mediated regulation of extracellular matrix accumulation. The Journal of biological chemistry. vol 279. issue 15. 2004-06-01. PMID:14742441. inhibition of calcineurin prior to the addition of tgf-beta revealed that calcineurin is required for tgf-beta-mediated accumulation of extracellular matrix (ecm) proteins but not cell hypertrophy. 2004-06-01 2023-08-12 Not clear
Fuad N Ziyade. Mediators of diabetic renal disease: the case for tgf-Beta as the major mediator. Journal of the American Society of Nephrology : JASN. vol 15 Suppl 1. 2004-05-25. PMID:14684674. treatment of diabetic mice with neutralizing anti-tgf-beta antibodies prevents the development of renal hypertrophy, mesangial matrix expansion, and the decline in renal function. 2004-05-25 2023-08-12 mouse
Fuad N Ziyade. Mediators of diabetic renal disease: the case for tgf-Beta as the major mediator. Journal of the American Society of Nephrology : JASN. vol 15 Suppl 1. 2004-05-25. PMID:14684674. these studies argue strongly in support of the hypothesis that overactivity of the tgf-beta system in the kidney is a crucial mediator of diabetic renal hypertrophy and mesangial matrix expansion. 2004-05-25 2023-08-12 mouse
Mohan R K Dasu, Hal K Hawkins, Robert E Barrow, Hui Xue, David N Herndo. Gene expression profiles from hypertrophic scar fibroblasts before and after IL-6 stimulation. The Journal of pathology. vol 202. issue 4. 2004-05-20. PMID:15095275. it is hypothesized that changes in the genes of cytokines, extracellular matrix proteins, and proteins regulating programmed cell death are related to hypertrophic scar formation. 2004-05-20 2023-08-12 Not clear
Mohan R K Dasu, Hal K Hawkins, Robert E Barrow, Hui Xue, David N Herndo. Gene expression profiles from hypertrophic scar fibroblasts before and after IL-6 stimulation. The Journal of pathology. vol 202. issue 4. 2004-05-20. PMID:15095275. no change in these matrix metalloproteinases could be shown with il-6 stimulation in hypertrophic scar fibroblasts. 2004-05-20 2023-08-12 Not clear
Mohan R K Dasu, Hal K Hawkins, Robert E Barrow, Hui Xue, David N Herndo. Gene expression profiles from hypertrophic scar fibroblasts before and after IL-6 stimulation. The Journal of pathology. vol 202. issue 4. 2004-05-20. PMID:15095275. the absence of any up-regulation of mmp-1 and mmp-3 in hypertrophic scar fibroblasts, in response to il-6, suggests that suppression of matrix metalloproteinases may play a role in the excessive accumulation of collagen formed in hypertrophic scars. 2004-05-20 2023-08-12 Not clear
Cynthia M Coleman, Rocky S Tua. Growth/differentiation factor 5 enhances chondrocyte maturation. Developmental dynamics : an official publication of the American Association of Anatomists. vol 228. issue 2. 2004-05-19. PMID:14517992. exposure to gdf5 significantly enhanced chondrocyte hypertrophy and maturation, as determined by the presence of alkaline phosphatase activity, collagen type x protein production, and the presence of a sulfated proteoglycan-rich extracellular matrix. 2004-05-19 2023-08-12 chicken
Guoyan Wang, Anita Woods, Shalev Sabari, Luca Pagnotta, Lee-Anne Stanton, Frank Beie. RhoA/ROCK signaling suppresses hypertrophic chondrocyte differentiation. The Journal of biological chemistry. vol 279. issue 13. 2004-05-07. PMID:14726536. rhoa overexpression in chondrogenic atdc5 cells results in increased proliferation and a marked delay of hypertrophic differentiation, as shown by decreased induction of alkaline phosphatase activity, mineralization, and expression of the hypertrophic markers collagen x, bone sialoprotein, and matrix metalloproteinase 13. 2004-05-07 2023-08-12 Not clear
Cornelia Piper, Heinz-Peter Schultheiss, Daniel Akdemir, Joern Rudolf, Dieter Horstkotte, Matthias Pauschinge. Remodeling of the cardiac extracellular matrix differs between volume- and pressure-overloaded ventricles and is specific for each heart valve lesion. The Journal of heart valve disease. vol 12. issue 5. 2004-04-27. PMID:14565712. different patterns of fibroblast-mediated remodeling of the extracellular matrix (ecm) might be expected between patients with pressure- and volume-induced left ventricular hypertrophy. 2004-04-27 2023-08-12 Not clear
Lee-Anne Stanton, Shalev Sabari, Arthur V Sampaio, T Michael Underhill, Frank Beie. p38 MAP kinase signalling is required for hypertrophic chondrocyte differentiation. The Biochemical journal. vol 378. issue Pt 1. 2004-04-22. PMID:14594450. in addition, p38 inhibition causes reduced expression of hypertrophic marker genes such as collagen x, matrix metalloproteinase 13 and bone sialoprotein. 2004-04-22 2023-08-12 mouse
Rethinasamy Prabhakar, Natalia Petrashevskaya, Arnold Schwartz, Bruce Aronow, Greg P Boivin, Jeffery D Molkentin, David F Wieczore. A mouse model of familial hypertrophic cardiomyopathy caused by a alpha-tropomyosin mutation. Molecular and cellular biochemistry. vol 251. issue 1-2. 2004-04-16. PMID:14575301. a dna hybridization microarray analysis of the transgenic vs. control ventricular rnas shows that 50 transcripts are differentially expressed by more than 100% during the onset of the hypertrophic process, many of which are associated with the extracellular matrix. 2004-04-16 2023-08-12 mouse
Mohammed Shakil Ahmed, Erik Øie, Leif Erik Vinge, Arne Yndestad, Geir Øystein Andersen G, Yvonne Andersson, Toril Attramadal, Håvard Attramada. Induction of myocardial biglycan in heart failure in rats--an extracellular matrix component targeted by AT(1) receptor antagonism. Cardiovascular research. vol 60. issue 3. 2004-04-16. PMID:14659801. cardiac remodelling associated with congestive heart failure typically involves dilatation of the ventricular cavities, cardiomyocyte hypertrophy and alterations of extracellular matrix. 2004-04-16 2023-08-12 rat